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ANTHROPOMETRIC MEASUREMENTS AND VITAL SIGNS COMPARED TO
IMAGING STUDIES IN HIGH RISK NEWBORNS
By
Ahmed Mostafa Hamed*, Fardous A. Abd El All***, Ahmad Fathy El-Gebaly*
Effat Abdel Moneim**, Hanan A Noaman*** and Nafessa Hasen***
Departments Of *Diagnostic Radiology, **Pediatrics, and *** Physiology,
Assiut Faculty of Medicine
ABSTRACT:
Our study was conducted on 81 high risk newborns 35 preterms, 46 fullterms) in
addition to 20 healthy newborns (9 preterms, 11 fullterms) as a control group matched with
study group. Anthropometric measurements (weight, length and head circumference) vital
signs (heart rate, systolic blood pressure, respiratory rate and temperature). Radiological
investigations were done for all cases and controls including transcranial sonar, brain CT, and
transcranial Doppler studies of internal carotid artery, middle cerebral artery and anterior
cerebral artery for mean velocity, pulsatility index and resistive index. The group of CNS
congenital anomalies showed significantly lower birth weight & significantly bigger head
circumference. The group of preterms with meningitis showed significantly bigger head
circumference. The group of preterms with HIE & the group of fullterms with meningitis
showed significantly lower HR. The groups of HIE (preterms & fullterms) as well as
complicated LBW showed significantly higher RR than controls . Higher percentage of
abnormalities was observed by CT than by transcranial sonar. IVH & PVE were found only
in preterms, PVE was not seen by CT while IVH and ventricular dilatation were equally seen
by sonar and CT. Brain oedema was over diagnosed by sonar than by CT. Other lesions
including cortical damage, WMH, meningeal enhancement and subarachnoid hemorrhage
were seen only by CT. Lower birth weight in preterms (<1220 gm) was significantly
associated with higher frequency of abnormal sonar & abnormal CT and IVH, also lower
birth weight in fullterms (<2750 gm) was significantly associated with higher frequency of
abnormal CT and ventricular dilation. Bradycardia (HR <120/m) was significantly associated
with significantly higher frequency of abnormal sonar &abnormal CT in our high risk
newborns (prerterms and fullterms) particularly significantly higher frequency of IVH in
preterms and WMH in fullterms. Hypotension in preterms (B.P. <45mmHg) was
significantly associated with significantly higher frequency of abnormal sonar & abnormal
CT , IVH and PVE, also hypotension in fullterms (B.P. <50mmHg) was significantly
associated with higher frequency of abnormal CT and WMH. Transcranial Doppler findings
revealed higher mean velocity and lower PI & RI in preterms and fullterms with HIE &
meningitis than controls. Also lower MV and higher PI & RI than controls. In preterms and
fullterms with bradycardia we observed higher MV and lower PI & RI. In preterms and
fullterms with hypotension, we observed lower MV and higher PI & RI . Significant -ve
correlations were observed between MV and HR, also significant +ve correlations were
observed between PI as well as RI and HR.
Conclusion: Transcranial sonar is very helpful in diagnosis of various CNS affection in high
risk newborns particularly in complicated LBW, HIE, meningitis and CNS congenital
anomalies. Higher rates of abnormalities both by transcranial sonar and CT were observed in
relation to bradycardia and hypotension. The use of transcranial Doppler may not reflect a
specific disease entity because it could be affected by other different factors.
KEY WORD:
Preterms
IVH
Transcranial ultrasound
ICH
PVE
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Transcranial Doppler CT
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ultrasonography. Presence of congenital
anomalies.
Weight, length, head circumference.
General examination including heart rate,
respiratory rate, temperature, colour.
Apnea, respiratory distress score, need for
oxygen therapy.
Abnormal movements, jitteriness or
convulsions (onset, type, frequency,
number and doses of anticonvulsants).
Neurological examination including conscious level, primitive reflexes, tone,
posture, tendon reflexes.
Systemic examination [chest, heart, abdominal examinations]
Presence of any birth injury.
Radiological Investigations were done for
all cases and controls on the third day of
life except for cases with meningitis who
mostly presented around the tenth day of
life.
INTRODUCTION:
The advent of cranial ultrasound as
a routine tool in neonatology greatly
improved our knowledge of the presence
and incidence of brain lesions in the
newborn infants1 .Cranial sonography is
used in the detection and follow up of
intracranial
hemorrhage,
ischemia,
congenital malformations and congenital
perinatal infection. Sonography, although
the most commonly used imaging
technique in neonates, is less sensitive and
less specific for the detection of intracranial ischemia and hemorrhage compared
with CT or MR imaging2. Diagnosis of
these conditions is important because,
although some are not treatable, they can
effect outcome. This information is
important for parental counseling1.
Transcranial Doppler has a number
of advantages as a method of evaluating
cerebral haemodynamics. It is relatively
cheap and non invasive, allowing repeated
measurements and continuous monitoring3. Doppler ultrasound may be helpful
in diagnosis of intraventricular hemorrhage, periventricular leukomalacia4. Also
Doppler US could be used in diagnosis of
infantile hydrocephalus,5
neonatal
seizures6 and pyogenic meningitis7.
Transcranial ultrasonography &
transcranial Doppler Ultrasound was
performed through the anterior fontanelle,
both in the coronal, axial and sagittal
planes using “high frequency” ultrasound
equipped with high frequency small
footprint 7.5 MHz, sector transducer
[Acuson XP 128 Machine ]. Routine
anterior coronal scan through the frontal
horns of the lateral ventricles was done.
The sylvian fissure appeared as Y-shaped
echogenic areas laterally. The lateral
ventricles were bordered by thalami,
which had an echogenecity similar to or
slightly less than that of adjacent
parenchyma. At the same scan by Doppler
mode the anterior cerebral arteries were
visualized in the sagittal fissure.
PATIENTS AND METHODS:
A longitudinal case/control study
was carried out during the period between
January 2005 to October 2005, the study
included 81 newborns who are considered
high risk newborns [35 were preterms and
46 were full terms]. The high risk
preterms were distributed as follows: [17
were LBW, 7 were with HIE and 11 were
with meningitis].The high risk full terms
were distributed as follows: [27 were with
HIE, 8 were with meningitis and 11 were
with CNS congenital anomalies] (HIE
cases were stage 2 or stage 3 according to
Sarnat and Sarnat, (1976)8. These high
risk newborns were selected from neonatal
ICU in Assuit University Hospital.
Gestational age was assessed by date of
the last menstrual period, antenatal
Coronal scan through the third
ventricle were done and at this level, the
choroid plexus were visualized in the floor
of both lateral ventricles and in the roof of
the third ventricle. Normal sized third
ventricle not usually visualized because
its transverse diameter was small and
middle cerebral artery in the sylvian
fissure could be visualized and Doppler
gate placed. At posterior coronal scan, the
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cerebellum appeared as an echogenic
midline structure in the posterior fossa.
Midline sagittal scan showed the cavum
septum pelluicdum as a comma shaped
fluid filled structure between the frontal
horns of the lateral ventricles. Cephalic to
the cavi septi, hypoechoic corpus callosum
seen that bordered superiorly by the
echogenic sulcus of corpus callosum,
which contained the pericallosual arteries.
Lateral sagittal images showed the
echogenic periventricular white matter
tracts and the brain parenchyma. Axial
scanning through the temporal bone was
used to evaluating the major branches of
the circles of Willis. The transducer was
placed on the lateral aspect of the head just
in front of the ear and above the
mandibular condyle.
Grade II, subependymal hemorrhage with
blood in non-dilated ventricles.
Grade III, subependymal hemorrhage with
blood in dilated ventricles.
Grade IV, subependymal hemorrhage,
blood in dilated ventricles, and
intraprenchymal blood.
Computed Tomography (CT) of the
Brain:- Done by using Toshiba Xpress/sx.
In most cases sedation was not required, in
restless patients the examinations was
done after feeding.
The following were looked for the
presence of cerebral edema, extra &
intracerebral
hemorrhage,
peri
&
intravenricular hemorrhage.
a. Assessment of ventricular size.
b. Presence of white matter and
cortical lesions.
c. Presence of congenital malformations.
d. Presence of post meningitic
complications as abscesses or
atrophic changes.
e. Presence of posterior fossa
pathology
or
subarachnoid
hemorrhage which are difficult to
asses by ultrasonography only.
f. Use
of
intravenously
administrated contrast material in
cases of meningitis.
Cerebral echogenicity: increased or
normal, homogenous or heterogeneous,
white/gray matter differentiation, presence
of hemorrhage, infarction or cystic
changes.
Width of the sulci, interhemispheric
fissure, sylvian fissures and extra cerebral
collections. Ventricular size and shape.
Three major cerebral arteries are
examined; the internal carotid artery,
[ICA], middle cerebral artery [MCA] and
the anterior cerebral arteries [ACA]. The
studied parameters were the mean velocity
“cm/sec” [MV], pulsatilty index [PI] and
resistive index [RI] for each artery. Our
imaging system could automatically
calculate the PI & RI with each Doppler
display sweep.
RESULTS:
Our study included 2 groups, 81
high risk newborns (35 preterms & 46
fullterms) as a study group and 20 healthy
neonates (9 preterms & 11 fullterms) as
control group .
The mean gestational age of the studied
group showed no significant difference to
the control group either preterms or
fullterms respectively.
The appearance of intracranial
hemorrhage (ICH) changed with time.
Acute hemorrhage ahs an echogencity
equal or similar to the choroids plexus. As
the blood clots lyses, it becomes
hypoechoic centrally, whereas the clots’
periphery is still echogenic.
According to Schillenger et al.,, 1988,
ICH divided into four grades9:
Grade I, subependymal hemorrhage only.
Transcranial sonar is a helpful
brain imaging modality in cases of
complicated LBW, HIE, meningitis and
CNS congenital anomalies. It is safe ,
cheap, accessible and does not need
transport of the baby. It is useful for
detection of IVH, PVE, ventricular dilation
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and brain edema. CT is more informative
of parenchymal brain lesions and
subarachnoid hemorrhage.
We also studied the relation
between transcranial Doppler values and
some factors in our high risk newborns. In
preterms and fullterms with bradycardia
we observed higher MV and lower PI &
RI. In preterms and fullterms with
hypotension, we observed lower MV and
higher PI & RI. Significant -ve
correlations were observed between MV
and HR, also significant +ve correlations
were observed between PI as well as RI
and HR. Significant –ve correlations were
observed between RI and systolic blood
pressure. The use of transcranial Doppler
may not reflect a specific disease entity
because it could be affected by other
different factors. A structural brain lesion
detected by transcranial sonar and or by
brain CT is more informative
than
transcranial Doppler as the latter results
depend on a wide variety of factors.
Higher percentage of abnormalities
was observed by CT than by transcranial
sonar. IVH & PVE were found only in
preterms, PVE was not seen by CT while
IVH and ventricular dilatation were
equally seen by sonar and CT. Brain
edema was over diagnosed by sonar than
by CT. Other lesions including cortical
damage, WMH, meningeal enhancement
and subarachnoid hemorrhage were seen
only by CT.
Transcranial Doppler findings
revealed higher mean velocity and lower
PI & RI in preterms and fullterms with
HIE & meningitis than controls. In cases
of congenital CNS anomalies (with
hydrocephalus) we observed lower MV
and higher PI & RI than controls .
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CASE PRESNTATIONS
Figure (1); Doppler criteria (wave forms)include mean velocity [MV], pulsatility index [PI] and
resistive index [RI]. These parameters were measured in internal carotid artery [ICA];( A) , middle
cerebral artery [MCA];(B) and anterior cerebral artery [ACA]; ( C ).
In our study, the higher readings of the mean velocity, PI and RI in ICA than in MCA and ACA
{both in the controls and cases either preterms or full terms}
Figure (2) (A) Sagittal images shows increased echogenecity in the cortex of the brain, gyri not
identified, ventricles compressed by edema (arrows), thalamus (th) and caudate nucleus (cau) seen.
(B ) Doppler spectral display an ischemic child, ant cerebral artery wave form, elevated diastolic
flow and decrease systolic flow, resistivity index 0.4 1.
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Figure (3): Grade I subependymal hemorrhage. (A) and ( B) sagittal sonogram show a focus of increased
echogenecity in the left subependymal area (arrows), just above the caudate nucleus. (C); the coronal image.
Figure (4): grade III hemorrhage(A) mid- sagittal sonar ( B) coronal images of preterms child coming with
dilated blood filled lateral ventricle and third ventricle forming so called ventricular cast. (C ) & (D) CT
appearance 3 days after showing the resolving hemorrhage.
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Figure (5) Post-menigetic hydrocephalus with ventricular septations seen in the body of the
right lateral ventricle. (A) mid sagittal sonogram. (B) coronal image.
Figure (6) Meningeal enhancement and ventriculitis On CECT.
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Figure (7) diffuse brain edema; (A) & (B), sagittal sonogram. (C) coronal sonogram show
diffuse white matter diffuse echogencity, mainly periventricular.
(D) & (F) The CT appearance, note the effacement of the sulci and diffuse white matter
hypodensity.
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Figure (8); Dandy walker variant;, hypoplastic vermis.
(A) coronal scan, large cyst seen central in the posterior fossa which
in fact dilated fourth ventricle
(B) Sagittal sonogram revealed associated hydrocephalus and the lateral
ventricle seen dilated.
(C ) & (D) comparative CT with normal sized posterior fossa and hypoplastic vermis and
small cerebellar hemispheres.
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dependent
part of the ventricle (the
occipital horns). It is difficult to identify
small mounts of hemorrhage in a non
dilated ventricle4. Color Doppler can
distinguish normal vascularized choroid
plexus
from nonvascularized clot.
Because the ventricles are dilated, grade
III hemorrhage is recognized more easily.
The blood may completely fill the lateral
ventricle, appearing as an echogenic cast
of the ventricle. Intraparenchymal blood
seen as an intensely echogenic focus in
the brain tissue (grade IV). Subarchnoid
and subdural hemorrhage s are similar to
include fluid collections over the brain
surface3.
DISCUSSION:
The clinical examination of the
central nervous system in the neonate is
often difficult with complex pathology.
Diagnostic imaging of the neonatal brain
has become extremely useful and has
developed along two main directions,
computerized tomography [CT] and
ultrasonography [US]. Cranial sonography
of the neonate is a widely accepted
technique for evaluating the neonatal
brain1, 9.
We studied
the frequency of
transcranial sonographic and CT findings
in our high risk newborns. Abnormal
sonographic findings were observed in
51.4% of preterms & 60.9% of full terms,
while Abnormal CT findings were found
in 65.7% of preterms & 80.4% of full
terms with no significant difference
(table-1).
Intraventricular hemorrhage
[IVH] was recorded in 17.1% of our high
risk preterms both by sonar and CT (table1). Ment (1999) mentioned that 75% of
cases of GMH/IVH are thought to be
clinically silent, although infants with
grade III and grade IV hemorrhage may
experience a significant decrease in
haematocrite, seizures, abnormal eye
findings and changes in tone and
reflexes(10). Bulas & Vezina (1999)
mentioned that sonography is excellent for
visualization of IVHs as CT4.
Periventricular
echodensities
[PVE] which represent early phase of
Periventricular
leukomalacia
were
recorded in 11.5% of our high risk
preterms by sonar only (table-1). PVE
were not discriminated by CT in our cases
since our sonar and CT were done on the
3rd day of life of our preterms where the
differentiation of acute lesion from normal
brain by CT may be difficult due to higher
water content of the brain. (Bulas &
Vezina, 1999) and , Barkovich & Truwit,
(1990) mentioned that during the acute
phase of PVL, CT may be normal or show
a subtle, low attenuation abnormality in
the periventricular region despite obvious
sonographic abnormalities4, 11.
Subepndymal hemorrhage appears
as a discrete
focus of increased
echogenecity above the caudate nucleus on
coronal views. Hemorrhage has no flow
signal on color Doppler sonography3.
Over period of days to weeks, grade I
hemorrhage liquefies and evolves into
subepndumal cyst. Isolated subependymal
grade I hemorrhage has virtually no
morbidity or mortality and more severer
grades of hemorrhage are associated with
poorer neurologic outcome. Grade II
hemorrhage results when the subependymal blood
ruptures through the
ventricular wall, entering the lumen. Most
often the
blood accumulates in the
The detection of IVH (28.6%),
PVE (28.6%) and brain edema (14.3%) by
sonar in our preterms with HIE (table-1)
was in agreement with Bulas & Vezina
(1999) who reported that asphyxia is an
important factor in the development of
IVH & PVL in the premature as it leads to
abolishment of autoregulation of cerebral
perfusion4.
The high frequency of brain edema
in our cases of fullterms with HIE detected
by sonar (44.4%) more than by CT
(37.1%) (table-1), is in agreement with
Enzmann (1997) who mentioned that when
the hypoxic event is severe enough, the
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ultrasound and CT scans will reflect the
mass effect caused by brain swelling and
consequent ventricular compression(12).
The relative high frequency of brain
edema detected by sonar may be related to
some false +ve results as increased
parenchymal echognicity may be caused
by other intermixing factors while brain
edema detected by CT is an accurate
report.
The appearance of uncomplicated
intracranial hemorrhage on computed
tomography is comparatively straightforward. On CT studies, fresh intracerebral
blood clots typically appear hyperdense
when compared to normal brain. High risk
babies, cerebral hemorrhage seen in the
subependymal region of the lateral
ventricle (germinal matrix region).
Germinal matrix region is a region of
very thin walled veins and actively
proliferating but transient cells located in
the subependymal layer of the lateral
ventricles. Germinal matrix hemorrhage is
probably cause by hypoxic-ischemic injury
to the deep vascular watershed zone in the
developing fetus. CT accurately depicts
acute hemorrhage and associated intraventricular or parenchymal hemorrhage.
Similarly, Leena et al., discussed
appearance and grading of the cerebral
hemorrhage.1, 9
The high frequency of ventricular
dilation recorded both by sonar and CT in
our cases of meningitis in preterms
(54.5%) and in full terms (25%) (table-1)
is in agreement with Cole (1998) who
mentioned that hydrocephalus can be
demonstrated in approximately 50% of
infants who die of meningitis13.
Also, all our cases of congenital
CNS anomalies revealed ventricular
dilation by sonar and by CT (100%) (table1). {With neural tube defects [63.6%] or
Dandy – walker malformation [18.2%] or
its variant [9.1%] or congenital aqueductal
stenosis (9.1%)}. Brown (1998) mentioned
that ultrasound can define ventricular size
and diagnose hydrocephalus, however it is
advisable to have a definitive CT or MRI
investigation14. So we can consider transcranial sonar as a helpful diagnostic tool of
perinatal brain insult in our cases as it is
non invasive, feasible easily accessible and
cheap.
Hypoxic-ischemic encephalopathy
(HIE) is the result of global rather than
focal brain injury. HIE is the consequence
of global perfusion or oxygentaion
disturbance. Two basic pattern are seen in
HIE are border zone infarcts and
generalized cortical necrosis. Ischemic
changes in HIE are concentracted
primarily along the arterial border-zones
between major cerebral and cerebellar
territories. Stoll and Kliegman discussed
HIE CT appearance. The most frequently
and severely affected area is the parietooccipital region. Basal ganglia are also
common site for HIE25. The most
common abnormalities observed in scans
are low density band o at the interface
between major vascular territories. Basal
ganglia and para-sagittal areas area the
most frequent sites. Initial CT scan may
be normal or minimally abnormal. Sever
generalized cerebral edema ensues over
24 to 48 hours and is seen as diffusely
low density brain. Sever atrophic changes
are common in surviving infants25 .
In our study, CT provides more
accurate informations about parenchymal
lesions and subarachnoid hemorrhage in
spite of its disadvantages that include
transport of high risk newborns, exposure
to irradiation and its cost. Four additional
findings were detected by CT and could
not be detected by sonar. These include
cortical damage, white matter hypodensity,
meningeal enhancement and subarachnoid
hemorrhage (table-1). Enzymann (1997)
mentioned that cortical damage could be
seen as loss of gray /white matter
distinction with abnormal low density on
CT12.
Allan & Riviello, (1992), described
white matter hypodensity that reflected
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acute cerebral hypoperfusion is diffuse
injury as areas of patchy low attenuation in
the white matter15. In cases of meningitis,
Gotoff, (2004), suggest that these areas it
represents cerebral infarction secondary to
vasculitis or thrombosis16. Cole (1998)
mentioned that varying degrees of
phlebitis and arteritis of intracranial
vessels can be found in all infants who die
of meningitis. Thrombophlebitis of veins
may occur in the subependymal zones13.
meningitis is associated with increasing
head circumference and bulging fontanel
and attributed that to ventricular dilation
which proved by stoppage of increase in
head circumference and the fontanel
became flat and soft after shunt
operation(19). Also, the mean head
circumference was significantly larger in
the group of full terms with congenital
CNS anomalies (38.18cm) than their
controls (35.63cm) with P < 0.05 (table-1).
Inoue et al., reported that the rapid
expansion of head circumference is a
presenting sign of CNS congenital
anomalies, this is attributable to
hydrocephalus20. This confirms our results
where all our full terms with congenital
CNS anomalies have ventricular dilation
by transcranial sonar.
Periventrcular leukomalecia is an
infarction of deep white matter adjacent to
the lateral ventricles. Initial sonographic
examination is commonly normal. Band
of increased periventricular echogencity
occurring within a day or tow of the
ischemic insult. Cystic encephalomalecia
( single or multiple cysts vary in size)
develop in periventrciular white matter 2
to 3 weeks after the acute insult. Similar
conclusions
discussed
by
other
investigators17.
Regarding
the
heart
rate,
significantly lower mean heart rate was
observed in our preterms with HIE
(129.57/m) than controls (141.44/m) with
P < 0.05. Also insignificantly low mean
heart rate in fullterms with HIE (132.7/m)
was observed (table-4). This is similar to
what reported by Gonzalez et al., who
concluded that bradycardia may be
frequent in infants with hypoxic ischemic
encephalopathy and that significant
association
between
cardiovascular
manifestations and all of the neurological
and extraneurological dysfunctions in
perinatal asphyxia is based on the severity
of hypoxic ischemic injury21. Also, there
was significantly lower mean heart rate
among our full terms with meningitis
(123.13/m) than their controls (136.75/m)
with P < 0.05 (table-4). This is in
agreement with Wang et al., and Perlman
et al., who reported that bradycardia is one
of the non specific signs of meningitis in
neonates22, 23.
We studied the anthropometric
measurements and vital signs in our high
risk newborns. Regarding the birth weight,
all the groups showed no significant
difference to the controls except for the
fullterm group with congenital CNS
anomalies who
showed significantly
lower mean birth weight (2523 grams)
than controls (3310 grams) with P < 0.05
(table-3) {where 68% of this group were
low birth weight}. This is similar to what
reported by Davidoff et al., who did a
retrospective analysis on those infants with
neural tube defects, they observed that
70% were low birth weight17. Similarly
Murshid et al., did prospective study on
cases of infantile hydrocephalus with
causes other than neural tube defects and
brain tumours, he revealed that 69% of all
studied patients were low birth weight18.
Regarding the respiratory rate
(RR), we observed significantly higher
mean RR in our preterms and fullterms
(51.7/m) & (43.28/M) than controls
(42.89/m) & (38.25/M) respectively with
P < 0.05 for each (table-1). This can be
The mean head circumference was
significantly larger for the preterm group
with meningitis (33.86 cm) than their
controls (30.67 cm) with P < 0.05 (table1). Okubo et al., reported that neonatal
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explained by significantly higher RR in
the group of complicated LBW
(49.94/m)than their controls (42.89/m)
with P < 0.05. This is in agreement with
Hack et al., who reported that a lot of
respiratory problems could occur in LBW
including respiratory distress syndrome,
pneumothorax, pneumome -diastinum,
interstital emphysema, congenital pneumonia, pulmonary hypoplasia, pulmonary
hemorrhage24.
cm/sec) than their controls (15 cm/sec) &
(17 cm/sec) respectively with P < 0.05 for
each and in PI of MCA in both preterms
(0.85) and fullterms (0.92) than their
controls (1.29) & (1.23) respectively with
P < 0.05 for each) (table-6). This is in
agreement with Stark & Seibert and Liao
& Hung who reported that a low resistive
index and an increase in velocity of
cerebral vessels occur in neonates with
asphyxia and could indicate a poor
prognosis27,28. Nishimaki et al., reported
that in unilateral neonatal cerebral
infarction with poor outcome, Doppler
studies demonstrated increases in cerebral
blood flow velocity but decreases in RI on
affected side29. Pryds and Co-workers
suggested
that
vasoparalysis
in
asphyxiated infants is the cause of low
resistance index shown by Doppler,
manifested as vasodilatation30.
Furthermore, the respiratory rate was
also significantly higher in our HIE cases
either preterms (60.28/m) or full terms
(56.33/m) than their controls (42.89/m) &
(38.25/M) respectively with P < 0.05 for
each (table-1). This is in agreement with
Stoll & Kliegman who reported that
among the systemic effects of asphyxia is
the pulmonary affection which could
include
pulmonary
hypertension,
pulmonary hemorrhage, or respiratory
distress syndrome25.
Our Doppler results in cases with
meningitis either preterms or fullterms
revealed higher mean velocity and lower
PI & RI in all examined arteries than their
controls (the difference was significant in
MV of MCA in preterms (21cm/sec) and
in PI of MCA in fullterms (0.91) than their
controls (15cm/sec) & (1.23) respectively
with P < 0.05 for each) (table-6). This is in
agreement with Goh & Minnus who
reported that in cases of pyogenic meningitis, there was a significant decrease in
the final resistance index due to significant
increase in the end diastolic velocity, there
was a significant increase in the final mean
flow velocity.7
In this work, we studied transcranial
Doppler values in our high risk newborns
and controls. The studied Doppler criteria
include mean velocity [MV], pulsatility
index [PI] and resistive index [RI]. The
pulsatility index and the resistive index
reflect the degree of distal resistance.
These parameters were measured in
internal carotid artery [ICA], middle
cerebral artery [MCA] and anterior
cerebral artery [ACA]. In our study, the
higher readings of the mean velocity, PI
and RI in ICA than in MCA and ACA
{both in the controls and cases either
preterms or full terms} (table-6) is in
agreement with Seibert et al., who
mentioned that mean velocity & RI are
higher in ICA than in small arteries26.
Although lower velocity and higher PI
& RI were observed in our cases of
congenital CNS anomalies (100% had
hydrocephalus) than their controls, yet the
difference was not significant (table-6).
Rennie reported that in infants with
hydrocephalus there were decreasing
velocities and an increased PI & RI5. Bode
& Eden explained these changes in the
cerebral blood flow in cases of
hydrocephalus that it could be due to either
stretching or increased resistance of the
Regarding the Doppler findings in our
groups of HIE, we observed higher mean
velocity, lower PI & RI of all examined
arteries in preterms and fullterms with HIE
than their controls (the difference was
significant in MV of ACA in both
preterms (24 cm/sec) and fullterms (34
254
EL-MINIA MED., BULL., VOL. 17, NO. 1, JAN., 2006
Hamed et al.,
__________________________________________________________________________________________
cerebral arteries and so both systolic and
end
diastolic
velocities
increase
31
significantly after decompression .
2. Blankenberg FG, Loh NN, Brocci
P, et al., (2000): Sonography, CT and MR
imaging; A prospective comparison of
neonates with suspected intracranial
ischemia and hemorrhage. American
Journal of Neuroradiolgy 21: 213218.
3. Markus HS (1999): Transcranial
Doppler ultrasound, J Neurol Neurosurg
Psychiatry; 67: 135137(August).
4. Bulas DI and Vezina GL (1999):
Preterm
anoxic
injury,
radiologic
evaluation, Radiologic Clinics of North
America, Vol. 37, No. 6.
5. Rennie JM (1997):
Neonatal
cerebral ultrasound, Cambridge University
Press, Cambridge.
6. Boylan GB, Panerai RB, Rennie
JM (1999): Cerebral blood flow velocities
in neonatal seizures, Arch Dis Child Fetal
Neonatal ed; 80: PF105-F110.
7. Goh D and Minnus RA (1993):
Cerebral blood flow velocity monitoring in
pyogenic meningitis, Archieves of Disease
in Childhood;68:111-119.
8. Sarnat H and Sarnat M (1976):
Neonatal encephalopathy following fetal
distress, A clinical and electroencephalographic study, Arch Neurol; 33: 696.
9. Schillenger D, Grant EG, Manz
HJ, et al., (1988): Intraparenchymal
hemorrhage in preterm neonates: a
broadening spectrum. AJNR 9:327-333.
10. Ment LR (1999): Intraventricular
hemorrhage in the preterm infant, (in)
McMillan JA, De Angelis CD, Feigin RD,
Warshaw JB (eds), Oski’s Pediatrics,
Principles & Practices (3rd ed) Lippinocott
Williams & Wilkins.
11. Barkovich AJ and Truwit C (1990):
Brain damage from perinatal asphyxia:
Correlation of MR findings with gestational age. AJNR Am J. Neuroradiol 11:
1087.
12. Enzmann DR (1997): Imaging of
neonatal hypoxic – ischemiccerebral
damage, in Stevenson DK, Sunshine P
(eds), Fetal and neonatal brain injury, 2nd
ed, Oxford University Press.
13. Cole
FS
(1998):
Bacterial
infections of the newborn,, in Taeusch
HW, Ballard RA (eds), Avery diseases of
We studied the transcranial Doppler
values in relation to heart rate and systolic
blood pressure in our high risk newborns.
We found higher mean velocity and lower
PI & RI in preterms and fullterms with
bradycardia than other cases (the
difference was significant in PI & RI of
MCA in preterms (0.61) & (0.59) and in PI
of MCA in fullterms (0.94) with
bradycardia than others without bradycardia (1.08) & (0.65) & (1.14)
respectively with P < 0.05 for each) (table7). Our results are in agreement with Katz
who mentioned that intracranial velocities
are reflections of an individual heart rate
and the examiners should be cautious
against taking a reading while the patient
is yawing, agitated or experiencing pain or
if there is any other reason causing a
change in heart rate(32). However, Bouma
& Muizelear mentioned that changes
resulting from cardiac output not
associated with hemodilution have little
effect on the cerebral blood flow if
autoregulation is intact33.
Lower velocity and higher PI & RI
were observed in preterms and fullterms
with hypotension (the difference was
significant in MV of ICA (35cm/sec) &
MCA (22cm/sec) in fullterms with
hypotension than those without hypotension (46 cm/sec) & (31 cm/sec)
respectively with P < 0.05 for each) (table8). This could reflect arterial vasosposm
secondary to low blood pressure which is
associated with decreased velocity and
increase in cerebrovascular resistance
which could cause focal brain ischemia,
according to Volpe explanation34.
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1. Leena H, Eugenio M, Frances C
(2000): Cranial ultrasound abnormalities
in fullterm infants in a postnatal word;
Outcome at 12 and 18 months. Arch.Dis
Child Fetal Neonatal Ed; 82, F128F133.
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the newborn, 7th ed, WB Saunders
Company, Philadelphia.
14. Brown JK (1998): Congenital
malformation of the central nervous
system, In Campell AGM and McIntosh N
(eds), Forfar and Arneils Textbook of
Pediatrics (5th ed), Churchill Livingstone.
15. Allan WC and Riviello JJ (1992):
Perinatal cerebrovascular disease in the
neonate, parenchymal ischemic lesions in
term and preterm infants, Ped Clin N Am,
Vol. 39( 4): 56-63.
16. Gottof SP (2004): Infections of
the neonatal infant, In Behrman RE,
Kliegman RM, Jenson HB (eds), Nelson
Textbook of Pediatrics (17hed) WB
Saunders.
17. Davidoff MJ, Petrini J, Damus K,
et al., (2002): Neural tube defects –
specific infant mortality in the united
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18. Murshid WR, Jarallah JS, Dad MI
(2000): Epidemiology of
infantile
hydrocephalus in Saudi Arabia, birth
prevalence and associated factors. Pediatr
Neurosurg, Mar; 32 (3): 11923.
19. Okubo T, Shirane R, Mashiyama S
(1984): Proteus mirabilis, brain abscess in
a neonate, No Shinkei Geka, Mar; 12 (3
suppl ): 394400.
20. Inoue R, Isono M, Kamido T, et
al., (2002); A case of schizencephaly with
subdural fluid collection in a neonate.
Childs Nerv Syst, Jul; 18 (67): 34850.
21. Gonzalez De Dios J, Moya M,
Castano C, et al., (1997): Clinical and
prognostic value of cardiovascular
symptoms in perinatal asphyxia. An Esp
Pediatr, Sep; 47 (3): 28994.
22. Wang SM, Liu CC, Tseng HW, et
al., (1999): Staphylococcus capitis
bacteremia of very low birth weight
premature infants at neonatal intensive
care units, clinical significance and
antimicrobial susceptibility. J Microbiol
Immunol Infect, Mar; 32 (1): 2632.
23. Perlman JM, Rollins N, Sanchez PJ
(1992): Late onset meningitis in sick very
low birth weight infants, clinical and
sonographic observations, Am J Dis Child;
146: 1297.
24. Hack M, Weissman B, Breslaw N,
et al., (1993): Health of very low birth
weight children during their first eight
years, J Pediat; 122:887.
25. Stoll GJ and Kliegman RM (2004):
High risk infant, in Behrman RE,
Kliegmaan RM, Jonson HB (eds), Nelson
Textbook of Pediatrics, 17th ed, Saunders.
26. Seibert Joanna J, Mc Gowman TC,
Chadduck WM, et al., (1990): Duplex
pulsed Doppler US versus intracranial
pressure in the neonate, clinical and
experimental studies, Radiology, 171: 155159
27. Stark JE and Seibert JJ (1994):
Cerebral artery Doppler ultrasonography
for prediction of outcome after perinatal
asphyxia, J Ultrasound Med;13:595-600.
28. Liao HT and Hung KL (1997):
Anterior
cerebral
artery
Doppler
ultrasonography for prediction of outcome
after perinatal asphyxia; Zhonghua Min
Guo Yiao Er Ke Yi Xue Hui Za Zhi, May Jun; 38 (3): 208-12.
29. Nishimaki S, Seki K, Yokota S
(2001). Cerebral blood flow velocity in
two patients with neonatal cerebral infarction. Pediatr Neurol/Apr; 24(4):320-3.
30. Pryds O, Greisen G, lou H, ET
AL., (1990): Vasoparalysis associated with
brain damage in asphyxiated term infants,
J Pediatr 117: 119-125.
31. Bode H and Eden A (1989):
Transcranial Doppler sonography in
children, Journal of Child Neurology;
4,Supplement P68-76.
32. Katz ML (2001): Intracranial
cerebrovascular evaluation, in Sandra L,
Hegan Ansert, Textbook of diagnostic
ultrasonography,
5th
ed,
Mosby,
California.
33. Bouma GJ, Muizelear JP (1990):
Relationship between cardiac output and
cerebral blood flow in patients with intact
and
impaired autoregulation. Dev Med
Child Neurol; 32 : 285
34. Volpe JJ (2001): Neurobiology of
periventricular leukomalacia in the
premature infant. Pediatr Res; 50: 55362.
256
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‫‪Hamed et al.,‬‬
‫__________________________________________________________________________________________‬
‫دراسة تقييم الوظائف الحيوية والتقييم اإلكلينيكي لألطفال حديثي الوالدة المعرضون‬
‫للخطر مقارنا بالتصوير الطبي للمخ‬
‫أحمد مصطفى حامد* ‪ -‬فردوس هانم عبد العال***‪-‬أحمد فتحي الجبالي* ‪-‬عفت عبد المنعم**‬
‫حنان أحمد نعمان*** ‪ -‬نفيسه حسن***‬
‫أقسام *األشعة التشخيصية ‪** -‬طب األطفال‪*** -‬الفسيولوجي ‪-‬كلية طب أسيوط‬
‫أجريتته هتتلد اسةرا ت ف ت م تشت أ أ تتيلج اسج ت م فت اس تتترم م ت ينت ير ‪ 2005‬حتتتأ أوتتتل ر‬
‫‪ 2005‬لقة اختير سلةرا لاحة لثم ني ج تً مت اسمرضت اسملجتلةي ةاختل اسرة يت اسمروتسم ت‬
‫األج ل أل ح سته حرج لم رضي سلخجر‪.‬‬
‫ت ف هلد اسةرا شرح سلةلر اس ل اسمه سلملج ه فلق اسصلتي ةل اسي فلخ سةرا اسمخ سهؤالء‬
‫األج ل لظهلر األةراض اسمرضي م نسيف ةرج تت اسمختل ت لقصتلر فت لصتلل استة لوتلس‬
‫االسته ب اس ح ئ ل ض م اس يلب اسخل ي سلمخ لقة ت ف هتلد اسةرا ت م رفت و ت ءم اسملجت ه فتلق‬
‫اسصلتي ةلأ اسمخ م خًل اسي فلخ لم خًل اسجمجم ةملمت فت تشتخيغ أ لتب اسحت اله و حتغ‬
‫ةقيتتو لم تتةئ سهتتلد اسحتت اله اسحرجتت استتت ةاختتل لحتتةم اسرة يتت اسمروتتسم لال ت تتتجيع اسختترلج متت‬
‫اسحض ن ه مم ي رضه سخجر أو ر إلا م ح لسن ن له سلحةم األش اسم ج يت لاستت أجريته سلحت اله‬
‫ةنة ث ه ح سته اسصحي ‪.‬‬
‫لأث ته اس حتغ أهميت اس حتغ سملجت ه فتتلق اسصتلتي ةلتأ اسمتتخ و تةيل م تةئ لمهت لرختيغ فت‬
‫فحغ هؤالء األج ل لتجرق اس حث إسأ اسةلر اسه سهلا اس حغ ف استشخيغ لألج قصلرد م رن‬
‫ألش اسم ج ي ‪.‬‬
‫يشول األج ل ن قص اسنمتل أقتل مت نصتف اسحت اله ‪ 35‬ج تً متنه ت ةشتر قليلت استلس لأحتة‬
‫ةشتتر ج تتً الستهت ب اس تتح ئ ينمت األج ت ل وت مل ‪ 46‬ج تتً اسنمتتل ثم نيت ف تتج ستهت ب اس تتح ئ‬
‫لأحة ةشر ج ً منه ت ةيتلب خل يت فت اسجهت س اس صت ‪ .‬أيضت لقتع االختيت ر ةلتأ ةشتري ج تً‬
‫‪ 9‬منه ن قص اسنمل لأحة ةشر و مل‬
‫ليم سيولنلا مجملة ه ونترلل ستم ةملي اإلحص ء اسج‬
‫اسنمل‬
‫لسهلد اسمجملة ه ت ةمل قي س سلشري اس ت ت استةاخل ‪ ICA‬لقيت س ترة مترلر استة ةاخلت‬
‫‪ Color Duplex‬لقي س مرلر اسة فت اسشتري اسمخت األمت م ‪ACA‬‬
‫جه س اسةل لر اسملل‬
‫لاألل ج ‪ MCA‬لقلرنه اسنت ئج سم ييس قية اسةرا سألج ل حةيث اسنمل مت لس ل ترة‬
‫ةق ه اس لب لم ةل ضغج اسة لقيت س ترة استتن س لخلصته اسم رنت ه إستأ استةلر اسمهت سلتةل لر فت‬
‫ةرا ت هتتؤالء األج ت ل ف ت ةرا ت شتتري استتة ف ت شتترايي اسمتتخ يتتة أن ت يتغيتتر تغيتتر تل ت اس لامتتل‬
‫لم ت ال تشخغ مرض ينت لوت م رنتت ت س حلغ األخترة خ صت اسملجت ه فتلق اسصتلتي‬
‫لاسلي يول اسجه س اسلي ي ل هم لاحة يحةة مةة اإلة ق لاستلقع اسم ت ل ستأثيره ةل نمل اسج ل‬
‫فيم ة‪.‬‬
‫ستشخيغ هتلد اسحت اله متع استرويتس ةلتأ ةلر اسملجت ه‬
‫لترم اسةرا إسأ م رف اس حلغ اسمن‬
‫فلق اسصلتي لاألش اسم ج ي مع م رن استشخيغ اسنه ئ سح س اس م سلج تل لاس ًمت ه اسحيليت‬
‫سلج ل اسلس ل رة اس لب ل رة استن س لضغج اسة ‪.‬‬
‫‪257‬‬